Dynamics of HPV16 DNA load reflect the natural history of cervical HPV-associated lesions

Monnier-Benoit, Sylvain; Dalstein, Véronique; Riethmuller, Didier; Lalaoui, Najoua; Mougin, Christiane; Prétet, Jean‐Luc

doi:10.1016/j.jcv.2005.09.001

Cited by 61 publications

(70 citation statements)

References 38 publications

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“…Recently, studies have focused on longitudinal observations of viral load to predict viral clearance or lesion progression (10,12). Initial data indicate that repeated measurements can improve prediction of persistence or clearance, but these data are, so far, limited to HPV16 only.…”

Section: Discussionmentioning

confidence: 99%

Human Papillomavirus Load Measured by Linear Array Correlates with Quantitative PCR in Cervical Cytology Specimens

et al. 2012

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Section: Discussionmentioning

confidence: 99%

Human Papillomavirus Load Measured by Linear Array Correlates with Quantitative PCR in Cervical Cytology Specimens

et al. 2012

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“…30,51 Our cross-sectional data also limit the evaluation of kinetics of the HPV 16 viral load, which may be more valuable in predicting CIN 2/3 and cervical carcinoma, as demonstrated in longitudinal studies that a higher viral load is highly predictive for precancerous lesion progression. 12,15 Periodic evaluation of the HPV viral load may be useful in monitoring viral clearing and predicting cervical precancerous lesion progression, but requires more studies to determine the value of HPV viral load as a predictive marker. 52,53 …”

Section: Discussionmentioning

confidence: 99%

“…[11][12][13][14][15][16] Integrating HPV 16 into the host genome of infected cells is considered a critical step for carcinogenesis. 17,18 HPV 16 integration promotes the transcription of E6 and E7 viral oncogenes.…”

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confidence: 99%

Distribution and viral load of eight oncogenic types of human papillomavirus (HPV) and HPV 16 integration status in cervical intraepithelial neoplasia and carcinoma

et al. 2007

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Current human papillomavirus (HPV) DNA testing using pooled probes, although sensitive, lacks specificity in predicting the risk of high-grade cervical intraepithelial neoplasia (CIN 2/3) progression. To evaluate selected HPV genotyping, viral load, and viral integration status as potential predictive markers for CIN progression, we performed HPV genotyping in formalin-fixed, paraffin-embedded cervical tissue with cervical carcinoma (29 cases) and CINs (CIN 1, 27 cases; CIN 2, 28 cases; CIN 3, 33 cases). General HPVs were screened using consensus primers GP5 þ /GP6 þ and PGMY09/11. HPV genotyping and viral load measurement were performed using quantitative real-time PCR for eight oncogenic HPV types (16, 18, 31, 33, 35, 45, 52, and 58). HPV 16 viral integration status was evaluated by measuring HPV 16 E2/E6 ratio. We observed that HPV DNA positivity increased in parallel with the severity of CINs and carcinoma, with 59% positivity in CIN 1, 68% in CIN 2, 76% in CIN 3, and 97% in carcinoma (P trend ¼ 0.004). The eight oncogenic HPV types were significantly associated with CIN 2/3 (81%) and carcinoma (93%) (odds ratio (OR), 15.0; 95% confidence interval (CI), 5.67-39.76; Po0.0001) compared with the unknown HPV types (OR, 2.87; 95% CI, 0.89-9.22; P ¼ 0.08). HPV 16 was the predominant oncogenic HPV type in CIN 2/3 (51%) and carcinoma (71%) and integrated significantly more frequently in carcinoma than in CIN 2/3 (P ¼ 0.004). No significant differences in viral load were observed across the disease categories. Our findings suggest that selected genotyping for the eight oncogenic HPV types might be useful in separating women with a higher risk of CIN progression from those with a minimal risk. We also conclude that the HPV 16 integration status has potential to be a marker for risk assessment of CIN progression.

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“…Use of PCR signal strength in this study allowed a first examination of viral load for the full range of anogenital HPV types in a true population-based cohort. Other studies primarily have focused on disease associations with HPV16 infection (9,(35)(36)(37)(38)(39) and a handful other individual HPV types (generally no more than 10 types in a single study; refs. 31, 40-43).…”

Section: Discussionmentioning

confidence: 99%

Relationships of Human Papillomavirus Type, Qualitative Viral Load, and Age with Cytologic Abnormality

et al. 2006

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Persistent cervical infections with carcinogenic human papillomaviruses (HPV) cause virtually all cervical cancer. Cytologic abnormalities are the manifestations of HPV infections used to identify women at risk. To compare the potential of the full range of anogenital HPV genotypes to induce cytopathic effects, we examined the influences of HPV type, viral load, and age on cytopathology among 1,222 women having a single HPV type at enrollment into a 10,000-woman population-based study in Costa Rica. Cervical specimens were tested for f40 HPV types by MY09/MY11 L1 primer PCR and type-specific dot blot hybridization. Types were organized by phylogenetic species and cancer risk. PCR signal strength served as a qualitative surrogate for viral load. Overall, 24.8% [95% confidence interval (95% CI), 22.4-27.3] of single prevalent HPV infections had concurrent abnormalities (atypical squamous cells or worse) ranging from 0.0% to 80.0% based on HPV type. Noncarcinogenic A3/A15 types, although highly prevalent, uncommonly caused cytologic abnormalities (13.1%; 95% CI, 9.8-17.0). In contrast, one quarter to nearly one half of infections with a single major carcinogenic species type (A9/A11/A7/A5/A6) produced abnormalities. Greater abnormalities were observed with increasing qualitative viral load of carcinogenic types; fewer abnormalities were observed among older women (>54 years). A high percentage (46.2%) of detected abnormalities in women infected with HPV16 or related A9 types were high grade or worse, consistent with strong carcinogenicity, compared with 10.7% in women infected with A7 types, including HPV18, a major cause of adenocarcinoma. The lack of evident severe abnormalities associated with HPV18 and related HPV types might have implications for screening for poorly detected glandular and A7-related lesions.

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Dynamics of HPV16 DNA load reflect the natural history of cervical HPV-associated lesions

Cited by 61 publications

References 38 publications

Human Papillomavirus Load Measured by Linear Array Correlates with Quantitative PCR in Cervical Cytology Specimens

Human Papillomavirus Load Measured by Linear Array Correlates with Quantitative PCR in Cervical Cytology Specimens

Distribution and viral load of eight oncogenic types of human papillomavirus (HPV) and HPV 16 integration status in cervical intraepithelial neoplasia and carcinoma

Relationships of Human Papillomavirus Type, Qualitative Viral Load, and Age with Cytologic Abnormality

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